The next decade should do for prostate cancer what the past one has done for breast cancer

MOST cancers are equal-opportunity killers. Some, though, are perforce sex-specific. Breast cancer is rare in men. And prostate cancer is obviously absent from women. Recent years have seen a plethora of new drugs—starting in 1998 with Herceptin—for treating breast tumours that are threatening to get out of control. No such breakthrough has happened with prostate cancer. Though easily treated if caught early, late-stage prostate cancer is serious and often fatal. But that may be about to change.

Better understanding of the biology of the disease, and particularly of the role of testosterone in promoting it, has stimulated a new era of drug development, reminiscent of the revolution that ushered in Herceptin. These novel treatments, which are now undergoing clinical trials, were one of the main topics of conversation at the Congress of the European Association of Urology, which took place in Paris on February 24th-28th.

Some of the therapies discussed remain conceptual almost to the point of fantasy: a genetically engineered virus that could destroy prostate-cancer cells from within, for example. Several, though, are already available, or are just about to be.

Cabazitaxel, made by Sanofi, a French firm, is one. It is a relative of taxol, a drug used to treat breast and ovarian cancer. It works by preventing the formation of structures called microtubules, which pull the chromosomes apart in dividing cells (such as cancer cells). It was approved for use in 2010 after trials showed that it could prolong the lives of men with late-stage disease. A second drug, abiraterone, made by Johnson & Johnson, an American company, was approved in 2011 after a trial was stopped because it had been so successful that the organisers deemed it unfair on those in the control group that they were not receiving the medicine too.

Abiraterone works by interfering with an enzyme involved in the production of testosterone. Crucially, it does so in all testosterone-producing tissues, particularly including the adrenal glands, not just the testes. A common change that occurs when prostate cells turn cancerous is that they become extremely sensitive to testosterone—so much so that late-stage prostate cancer is often referred to as being “castration-resistant”, because even that drastic testosterone-reducing treatment cannot halt it. But abiraterone can.

Testosterone poisoning

Cutting off the testosterone supply is not, however, the only approach possible. MDV3100, made by Astellas, a Japanese firm, and Medivation, an American one, reduces the cancer's sensitivity to what testosterone is already there. This drug, not yet approved for prescription, works by gumming up testosterone receptors on the cancer cells' surfaces, so they cannot react to the hormone. It also cuts the lines of communication between any receptors which are still activated and the cell nucleus, so that the nucleus cannot take instructions from the hormone.

A fourth drug, alpharadin, developed by Algeta, a Norwegian firm, has a completely different mechanism of action. It works not on the primary cancer but on one of its most dangerous consequences, secondary bone tumours. Ironically, its active ingredient is radium, a substance more usually thought of as a cause of cancer than as a treatment. But one reason radium is dangerous is that, as a glance at the periodic table will show, it is chemically similar to calcium, a principal ingredient of bone. It therefore gets absorbed by bones if ingested, rather than being excreted.

Algeta's researchers have exploited this to produce a drug that is taken up by bones. In someone who already has cancer that is a good thing, because the radiation produced kills the cancer cells, and the drug gets concentrated where it is needed most.

It sounds desperate, and it is. But it seems to work. A trial at the Royal Marsden Hospital, in London, was stopped last year for the same reasons that the abiraterone trial was stopped: the treatment was too successful to deny it to the control group. Alpharadin is now, therefore, awaiting approval by the authorities.

The final proven approach to castration-resistant prostate cancer is a vaccine. This is not a prevention, in the way that most vaccines are, but a treatment for existing disease. Sipuleucel-T, as the vaccine in question is known, is made by Dendreon, an American firm. The starting point is a culture of human dendritic cells. These are part of the immune system and, if suitably treated with a substance called a fusion protein, can be used to make prostate-cancer cells vulnerable to immune attack.

Sipuleucel-T's main drawback is that each treatment has to be handcrafted to the individual receiving it, using dendritic cells from his own body. This is hugely expensive—almost $100,000 a course. That is a sum which insurance companies and government health services might understandably be reluctant to fork out.

Cost, indeed, is a consideration for others among the new anti-prostate-cancer treatments. Britain's National Institute for Health and Clinical Excellence, which assesses the cost-effectiveness of new medicines that might be paid for by the country's National Health Service, reckons, for example, that abiraterone is too expensive to justify the extra months of life it brings. But Herceptin, too, was subject to scrutiny about its cost at the beginning. Now Herceptin treatment is routine, and many women's lives are the better (and longer) for it. With luck, in a few years' time, men will be able to say the same.